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1.
Biochemistry ; 54(43): 6555-66, 2015 Nov 03.
Artículo en Inglés | MEDLINE | ID: mdl-26465056

RESUMEN

The Hippo pathway was originally identified and named through screening for mutations in Drosophila, and the core components of the Hippo pathway are highly conserved in mammals. In the Hippo pathway, MST1/2 and LATS1/2 regulate downstream transcription coactivators YAP and TAZ, which mainly interact with TEAD family transcription factors to promote tissue proliferation, self-renewal of normal and cancer stem cells, migration, and carcinogenesis. The Hippo pathway was initially thought to be quite straightforward; however, recent studies have revealed that YAP/TAZ is an integral part and a nexus of a network composed of multiple signaling pathways. Therefore, in this review, we will summarize the latest findings on events upstream and downstream of YAP/TAZ and the ways of regulation of YAP/TAZ. In addition, we also focus on the crosstalk between the Hippo pathway and other tumor-related pathways and discuss their potential as therapeutic targets.


Asunto(s)
Proteínas Adaptadoras Transductoras de Señales/metabolismo , Neoplasias/metabolismo , Factores de Transcripción/metabolismo , Proteínas Adaptadoras Transductoras de Señales/genética , Animales , Regulación de la Expresión Génica , Proteínas Hedgehog/metabolismo , Humanos , Hipoxia/metabolismo , Sistema de Señalización de MAP Quinasas , Ácido Mevalónico/metabolismo , MicroARNs/genética , MicroARNs/metabolismo , Modelos Biológicos , Neoplasias/genética , Fosfatidilinositol 3-Quinasas/metabolismo , Procesamiento Proteico-Postraduccional , Proteínas Serina-Treonina Quinasas/metabolismo , ARN Neoplásico/genética , ARN Neoplásico/metabolismo , Receptores Androgénicos/metabolismo , Receptores Acoplados a Proteínas G/metabolismo , Receptores Notch/metabolismo , Transducción de Señal , Proteínas Smad/metabolismo , Factores de Transcripción/genética , Vía de Señalización Wnt
2.
Gene ; 575(1): 1-8, 2016 Jan 01.
Artículo en Inglés | MEDLINE | ID: mdl-26341058

RESUMEN

Hypoxic regions are common in solid tumors and have an impact on tumor progression and on the therapeutic response. However, the underlying mechanism for hypoxic tumor microenvironment has not been entirely elucidated. Recently, long noncoding RNAs (lncRNAs) are being increasingly recognized to contribute to carcinogenesis through diverse mechanisms. To date, several lncRNAs have been described in hypoxia-associated cancer process, implying a potential role in maintaining cellular homeostasis and enabling an adaptive survival under hypoxic stress conditions. While it has been widely accepted that a complex cellular network of gene products, such as protein and miRNA, take part in hypoxic cancer progression, it remains largely elusive how lncRNAs participate in it. In this review, we introduce an update view of lncRNAs, focusing on hypoxia-related lncRNAs. We hereby summarize the cause and consequence of hypoxia-modulated lncRNAs in cancer as well as their functional mechanisms, highlighting the specific roles of lncRNAs in hypoxia response in cancer.


Asunto(s)
Neoplasias/metabolismo , ARN Largo no Codificante/metabolismo , ARN Neoplásico/metabolismo , Animales , Hipoxia de la Célula , Humanos , Neoplasias/genética , ARN Largo no Codificante/genética , ARN Neoplásico/genética
3.
J Neurol Sci ; 366: 127-134, 2016 Jul 15.
Artículo en Inglés | MEDLINE | ID: mdl-27288790

RESUMEN

Since Alzheimer's disease (AD) is becoming the prevalent dementia in the whole world, more underlying mechanisms are emerging. Long time has the transcription factor NF-κB been identified to participate in AD pathogenesis, various studies have focused on the causes and effects of AD that are linked to NF-κB. In this review we discuss diverse environmental stimuli including oxidative stress, neuroinflammation and metabolism, involved signaling pathways such as PI3K/AKT, MAPK and AGE/RAGE/GSK-3 and newly found ncRNAs that mediate neuron toxicity or neuron protection through NF-κB activation and the following response associated with the same factors in AD. These may provide future orientation of investigation at transcription level and support efficient treatment to AD by a better understanding of the upstream regulators and downstream effectors of NF-κB.


Asunto(s)
Enfermedad de Alzheimer/metabolismo , FN-kappa B/metabolismo , Enfermedad de Alzheimer/tratamiento farmacológico , Animales , Humanos
4.
Gene ; 547(1): 1-9, 2014 Aug 15.
Artículo en Inglés | MEDLINE | ID: mdl-24967943

RESUMEN

Over the past fifteen years, small regulatory RNAs, such as siRNA and miRNA, have been extensively investigated and the underlying molecular mechanisms have been well documented, suggesting that ncRNAs play a major function in many cellular processes. An expanding body of evidence reveals that long non-coding RNAs (lncRNAs), once described as dark matter, are involved in diverse cellular progresses, including regulation of gene expression, dosage compensation, genomic imprinting, nuclear organization and nuclear-cytoplasm trafficking via a number of complex mechanisms. The emerging links between lncRNAs and diseases as well as their tissue-specific expression patterns also indicate that lncRNAs comprise a core transcriptional regulatory circuitry. The function of lncRNAs is based on their sequence and structure; and they can combine with DNA, RNA, and proteins both in the nucleus and the cytoplasm. However, detailed insights into their biological and mechanistic functions are only beginning to emerge. In this review, we will mainly talk about diverse ways of action of lncRNAs in different sub-cellular locations and provide clues for following studies.


Asunto(s)
Núcleo Celular/genética , Citoplasma/genética , ARN no Traducido/fisiología , Impresión Genómica , Humanos
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